Appeal overturns link between multiple sclerosis and whiplash

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The nervous system has conclusively been discerned as one which
mediates the immune response. I wrote a paper concerning this point over
fifteen years ago, along with documentation from scientific studies from
around the world. Trauma to the cervical spine can most assuredly create
malpositions/aberrent motions of this region with an accompanying
inflammation effecting nerve pressure/interference associated with the
causation/exacerbation of abnormal immune system responses. I would also
look to a possible underlying copper/zinc/iron nutritional imbalance, and
on a more basic level, agnesium/calcium balance implicating also
potassium, with accompanying dehydration.

There are various anecdotal reports about clinical attacks developing
after trauma in multiple sclerosis (MS) patients. However, there are no
statistical or epidemiological data showing that the relation between
trauma and MS is more than coincidental. It is quite difficult to claim
trauma as a possible causal factor in MS, in the lack of sufficient
pathophysiological clues (1,2).

There are, indeed, some clues that trauma may somehow be related with MS.
The association between MS and trauma seems to be closely related with
blood brain barrier (BBB). Myelin antigens can not be presented to the
immune cells in thymus during foetal life because of this barrier between
blood and central nervous system (CNS). So, an autoimmune response against
myelin sheet develop in case of an exposure of these antigens to immune
system cells in the blood. Trauma is claimed to alter BBB permeability and
thus give rise to the recognition of CNS antigens by the immune system.

There is a similar condition called autoimmune orchitis, in which
testicular cells are damaged by inflammatory infiltrates, giving rise to
infertility in male patients. There is also a barrier between testis and
blood and testicular antigens are not recognised by thymus in the foetal
life, just like CNS antigens. Trauma or surgery has so far been claimed to
play a causal role in blood-testis barrier dysfunction, which causes
antigens to be exposed to patient's own immune system (3,4).

On the other hand, there is a growing body of evidence indicating that
mitochondrial (mt) DNA mutations may contribute to genetic susceptibility
in MS. Leber's hereditary optic neuropathy (LHON) is characterised by
progressive visual loss and is related with several mt DNA mutations
(5,6). An increasing number of case reports about LHON patients presenting
with clinical and neuroimaging (MRI) findings of MS raised the possibility
that mt DNA mutations may be a pathogenic factor in MS (7,8). However,
recent data has revealed that mutations related with LHON are observed in
only a restricted number of MS patients, especially those with typical MS
and classical DNA mutations do not contribute to the etiology of a large
group of patients with typical MS (9). These findings do not rule out mt
DNA mutations as a possible causal factor in MS and further mutations can
not be excluded in MS (7).

The capillary endothelium of BBB contrasts with other endothelial cells in
having tight junctions, low permeability to solutes and a high density of
mitochondria (10). Increased mt density in BBB capillaries aid in
maintaining ionic gradients across the barrier and thus provide a stable
environment for brain functions (11). Alterations in BBB permeability are
important in the pathophysiology of MS and mt contents have been
demonstrated to decrease in rats with slight clinical findings of
experimental autoimmune encephalomyelitis (laboratory counterpart of MS)
and sharply decline with further worsening of clinical signs (12,13). It
has also long been established that CNS mt levels tend to decline shortly
after traumatic brain injury (14). These observations implicate a possible
role for mt dysfunction in development of clinical signs of MS after
trauma. Trauma may be an additional stress factor for mt functions in MS
cases with existing BBB permeability dysfunction and autoimmune reaction
observed in MS may even be secondary to BBB dysfunction due to pre-
existing mt DNA mutations, at least in a small portion of MS cases.
Nevertheless, the association of trauma, MS and mt dysfunction needs to be
further elucidated by future researches.

It is quite logical to accept that it is currently hard to establish the
relation of trauma with MS in individual cases. Trauma may be a causal
factor at least in some of the patients, however "it would not cause MS by
itself but could bring on the condition in already susceptible
individuals" (1), as implicated previously.

I have had relapsing remitting MS for about 12 years now. I have had
3 exacerbations from which I had completely recovered. Then, I was in a
car accident where a car struck us from behind going about 40 mph.
Immediately, I had only felt dizzy. The next day, the numbness began in
my pinky finger on the right side and progressed to my ankle over a few
week period. All on the right side. Although I am not ever anxious to
take medications, I did resort to 500mg of SoluMedrol for 5 days IV. This
did arrest the progress of the debilitation. The accident was 5/28/99.
To date, the tingling and numbness remain from the top of my head to my
waist, all on the right side. I am a single mother and the only
"breadwinner" for our family. As I was a hairdresser for 20+ years, and
cannot feel my right hand, that job has become impossible. I am searching
for information and articles that support the theory that whiplash and
cervical trauma can exacerbate MS. Please help me. Thank you. Beth

I was involved in a minor car accident where the van that I was in
was hit from behind. The damage to the vehicle was very minimal but the
trauma to my neck being slung backwards rapidly and then forward was
extremely painful. Since it was my parents driving I pretended that I was
alright. The following day I started into a relapse with my MS which never
subsided. That was a year and a half ago. I have full body numbness,
spasticity, ON and bladder problems. There is no doubt in my mind that the
car accident caused this. Prior to the accident I had been working full
time with very limited symptoms. Now I am on disability.